Fig. 5. Human Shn1 can compensate for loss of Shn function in Drosophila embryogenesis. Lateral views of Drosophila embryos showing brk-lacZ expression at stage 13 (left), and darkfield images of differentiated cuticle (right). Anterior left, dorsal up. (A) In wild-type embryos, the brk-lacZ reporter is expressed ventrally but is downregulated in the dorsal ectoderm (de, vertical bar) in response to Dpp signaling. (B) In wild-type animals, the thoracic and abdominal segments differentiate denticle belts (arrowhead) characteristic of the ventral epidermis, whereas the dorsal epidermis contains fine dorsal hairs (arrow). (C,D) In shn mutants, brk-lacZ expression is derepressed (C), and the cuticle displays a characteristic `dorsal open' phenotype (arrow) owing to the failure of dorsal epidermal differentiation (D). (E-H) Rescue of shn^P4738 null embryos by UAS-Shn and UAS-hShn1. In control experiments, a UAS-Shn transgene driven by the heat-shock Gal4 driver can respond to endogenous Dpp signaling and repress brk-lacZ expression in the dorsal ectoderm (E). It can also rescue the morphological defects in shn^P4738 mutants (F). Rescued embryos differentiate a dorsal ectoderm and therefore show a closed and contiguous dorsal cuticle. Remarkably, UAShShn1 is as effective as Drosophila Shn in compensating for the loss of endogenous Shn function (compare G,H with E,F).